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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

F-box protein 7

FBXO7, PARK15, Fbx7, F-box protein 7, FBX07
This gene encodes a member of the F-box protein family which is characterized by an approximately 40 amino acid motif, the F-box. The F-box proteins constitute one of the four subunits of the ubiquitin protein ligase complex called SCFs (SKP1-cullin-F-box), which function in phosphorylation-dependent ubiquitination. The F-box proteins are divided into 3 classes: Fbws containing WD-40 domains, Fbls containing leucine-rich repeats, and Fbxs containing either different protein-protein interaction modules or no recognizable motifs. The protein encoded by this gene belongs to the Fbxs class and it may play a role in regulation of hematopoiesis. Alternatively spliced transcript variants of this gene have been identified with the full-length natures of only some variants being determined. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Ubiquitin, ATP13A2, E3 ubiquitin ligase, PINK1, DJ-1
Papers using FBXO7 antibodies
Phosphorylation by Akt1 promotes cytoplasmic localization of Skp2 and impairs APCCdh1-mediated Skp2 destruction
Kyprianou Natasha, In PLoS ONE, 2008
... Rabbit antibodies: Emi1, Millipore; Fbx4, Rockland (Gilbertsville, PA); Fbx7, Fbx31, Novus Biologicals; Flag, Nedd8 and Sirt1, ...
Papers on FBXO7
F-box protein 7 mutations promote protein aggregation in mitochondria and inhibit mitophagy.
Tan et al., Singapore, Singapore. In Hum Mol Genet, Dec 2015
The mutations of F-box protein 7 (FBXO7) gene (T22M, R378G and R498X) are associated with a severe form of autosomal recessive juvenile-onset Parkinson's disease (PD) (PARK 15).
A new F-box protein 7 gene mutation causing typical Parkinson's disease.
Brice et al., ─░stanbul, Turkey. In Mov Disord, Jul 2015
BACKGROUND: Recessive mutations in the F-box protein 7 gene (FBXO7; PARK15) have been identified as a cause of the parkinsonian-pyramidal syndrome.
Defective erythropoiesis in a mouse model of reduced Fbxo7 expression due to decreased p27 expression.
Laman et al., Cambridge, United Kingdom. In J Pathol, Jul 2015
Recent genome-wide association studies in human populations have associated several SNPs near or within FBXO7 with erythrocyte phenotypes.
Neuroimaging studies and whole exome sequencing of PLA2G6-associated neurodegeneration in a family with intrafamilial phenotypic heterogeneity.
Lee et al., Anyang, South Korea. In Parkinsonism Relat Disord, Apr 2015
Analysis of the non-synonymous SNVs that were not shared between the two family members revealed non-synonymous SNVs related to parkinsonism including a novel heterozygous mutation (p.T44N) in FBX07 (PARK15) only in the proband, and non-synonymous SNVs related to neurodegeneration with brain iron accumulation in the affected brother.
Status of the Parkinson's disease gene family expression in non-small-cell lung cancer.
Dai et al., Chongqing, China. In World J Surg Oncol, 2014
PARK15, and 99/114 (86.84%) glucocerebrosidase (GBA).
The FP domains of PI31 and Fbxo7 have the same protein fold but very different modes of protein-protein interaction.
Du et al., Carbondale, United States. In J Biomol Struct Dyn, 2014
Fbxo7 and PI31 contain a conserved FP domain that mediates the homo-/hetero-dimerization of the proteins.
A new Turkish family with homozygous FBXO7 truncating mutation and juvenile atypical parkinsonism.
Elibol et al., Ankara, Turkey. In Parkinsonism Relat Disord, 2014
Among these, homozygous or compound heterozygous mutations in the F-box only protein 7 gene (FBXO7) cause juvenile parkinsonism with variable degrees of pyramidal disturbances (PARK15).
FBXO7-R498X mutation: phenotypic variability from chorea to early onset parkinsonism within a family.
Ertan et al., ─░stanbul, Turkey. In Parkinsonism Relat Disord, 2014
OBJECTIVE: FBXO7 mutations (PARK 15), first reported in 2008, are among the monogenic causes of early-onset parkinsonism.
FBXO7 Y52C polymorphism as a potential protective factor in Parkinson's disease.
Wu et al., Taipei, Taiwan. In Plos One, 2013
Mutations in the F-box only protein 7 gene (FBXO7), the substrate-specifying subunit of SCF E3 ubiquitin ligase complex, cause Parkinson's disease (PD)-15 (PARK15).
Mutations in the ATP13A2 gene and Parkinsonism: a preliminary review.
Xu et al., Chengdu, China. In Biomed Res Int, 2013
PD appears to be caused by genetic and environmental factors, and pedigree and cohort studies have identified numerous susceptibility genes and loci related to PD. Autosomal recessive mutations in the genes Parkin, Pink1, DJ-1, ATP13A2, PLA2G6, and FBXO7 have been linked to PD susceptibility.
Beyond ubiquitination: the atypical functions of Fbxo7 and other F-box proteins.
Laman et al., Cambridge, United Kingdom. In Open Biol, 2013
We review Fbxo7 as an exemplar of this special group as it has well-defined roles in both SCF and non-SCF complexes.
The genetics of Parkinson's disease: progress and therapeutic implications.
Bonifati et al., Bethesda, United States. In Mov Disord, 2013
Notably, whereas most mutations, such as those in SNCA, PINK1, PARK2, PARK7, PLA2G6, FBXO7, and ATP13A2, are a rare cause of disease, one particular mutation in LRRK2 has been found to be common in certain populations.
F-box only protein 7 gene in parkinsonian-pyramidal disease.
Jankovic et al., Changsha, China. In Jama Neurol, 2013
Among them, PARK15 -associated parkinsonism, also referred to as parkinsonian-pyramidal disease (PPD), was found to be caused by mutations in the F-box only protein 7 gene (FBXO7).
Early-onset autosomal-recessive parkinsonian-pyramidal syndrome.
Wu et al., Taipei, Taiwan. In Acta Neurol Taiwan, 2012
However, mutations inATP13A2, PLA2G6 and FBX07 are often associated with rapidly progressive parkinsonism and with additional features including pyramidal signs, cognitive decline and loss of sustained Levodopa responsiveness.Clarifying the phenotypes of each of these autosomal-recessive parkinsonian-pyramidal syndromes and understanding the mechanism ot these causative gene products might illuminate the pathogenesis of dopaminergic neuronal degeneration also in the common forms of PD.
Lack of association between three single nucleotide polymorphisms in the PARK9, PARK15, and BST1 genes and Parkinson's disease in the northern Han Chinese population.
Pang et al., Shenyang, China. In Chin Med J (engl), 2012
The SNPs investigated in the BST1, PARK15 and PARK9 genes associated with PD susceptibility are not associated with PD in the northern Han Chinese population.
Knockdown of Fbxo7 reveals its regulatory role in proliferation and differentiation of haematopoietic precursor cells.
Laman et al., Cambridge, United Kingdom. In J Cell Sci, 2011
The physiological effect of reduced levels of Fbxo7 in mice showed significantly increased pro-B cell and pro-erythroblast populations, consistent with Fbxo7 having an anti-proliferative function and/or a role in promoting maturation of precursor cells.
A Competitive binding mechanism between Skp1 and exportin 1 (CRM1) controls the localization of a subset of F-box proteins.
Laman et al., Cambridge, United Kingdom. In J Biol Chem, 2011
Skp1 binding prevented Fbxo7 from contacting CRM1.
A conserved F box regulatory complex controls proteasome activity in Drosophila.
Steller et al., New York City, United States. In Cell, 2011
DmPI31 binds Nutcracker via a conserved mechanism that is also used by mammalian FBXO7 and PI31.
Loss of nuclear activity of the FBXO7 protein in patients with parkinsonian-pyramidal syndrome (PARK15).
Bonifati et al., Rotterdam, Netherlands. In Plos One, 2010
activity of FBXO7 in the nucleus appears therefore crucial for the maintenance of brain neurons and the pathogenesis of PARK15
Expression of Fbxo7 in haematopoietic progenitor cells cooperates with p53 loss to promote lymphomagenesis.
Laman et al., Cambridge, United Kingdom. In Plos One, 2010
Fbxo7 negatively regulates the proliferation and differentiation of haematopoietic progenitor cells in a p53-dependent manner
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